There is no cell system in current usage that has a uniform radiosensi
tivity for the production of chromatid-type aberrations. Consequently,
aberration frequencies fluCtuate with sample-time after exposure; the
re is no unique yield to set against absorbed dose. Given this situati
on, the observed yields, and their time-profiles, are subject to modif
ication by cell kinetic factors, in particular, the mitotic delay whic
h inevitably accompanies all clastogenic treatments. This paper discus
ses some cell-cycle modelling methods which attempt to explore the eff
ects of these perturbations on aberration frequencies, and which, in t
ime, may alloW us to correct observed yields to obtain reliable, and u
seable, scores of chromatid structural changes.